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Expression data from mouse skin treated with a miR-29 mimic or a miR-29 inhibitor

ABSTRACT: Expression data from mouse skin treated with a miR-29 mimic or a miR-29 inhibitor

PROVIDER: PRJNA438999 | ENA |

REPOSITORIES: ENA

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Expression data from mouse skin treated with a miR-29 mimic or a miR-29 inhibitor

Project description:We performed a microarray analysis of mouse skin treated with a miR-29b mimic or a miR-29 inhibitor in order to identify pharmacodynamic (PD) biomarkers that were reciprocally regulated in vivo in the skin

2018-11-27 | GSE112044 | GEO

miR-29 mimic and inhibitor expression in the clear cell renal cell carcinoma cell lines 786-O, A-498 and ACHN

Project description:The goal of this study was to investigate the regulatory events underlying post-transcriptional changes in gene expression in cancer. We observed that the miR-29 regulon had reccurently increased mRNA stability across multiple cancer types and hypothesized that its down-regulation is responsible at least in part for alterations in the cancer transcriptome. To verify if restoring miR-29 activity can partially reverse these changes, we expressed a miR-29 mimic in the 786-O and A-498 clear cell renal cell carcinoma (ccRCC) lines and performed RNA-sequencing on extracted RNA. We computed differential gene expression in the cell lines expressing the miR-29 mimic, compared to the control sample. We observed that expression of miR-29 mimic partially shifts the transcriptome of cells toward a normal cell state, primarily by down-regulating the majority of genes that are up-regulated in ccRCC tumors, most of which are also miR-29 targets. We observed opposite trends when expressing a miR-29 inhibitor in the ACHN ccRCC cell line. The results suggest that miR-29 downregulation is responsible for changes in the mRNA stability of a considerable number of genes in ccRCC, which can be partially rescued when miR-29 activity is restored.

2022-07-19 | GSE145088 | GEO

Expression data from human macrophages treate with miR-1246 mimic/inhibitor

Project description:MiR-1246 was found to promote tumorigenesis and metastasis in sevearl cancer types. In the context of tumor microenvironment, tumor-associated macrophages are a central part typically correlated with poor prognosis. We used microarray data to determine the gene expression profile in M2-like macrophages when treated with an overexpression of miR-1246 (conducted by miR-1246 mimic). As controls, we used either scambaled mimic control sequence, or a miR-1246 inhibitor.

2018-03-27 | GSE107870 | GEO

Expression data from human macrophages treate with miR-1246 mimic/inhibitor

Project description:Expression data from human macrophages treate with miR-1246 mimic/inhibitor

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A Genomic Portrait of the Genetic Architecture and Regulatory Impact of microRNA Expression in Response to Infection (functional investigation of the role of miR-29)

Project description:Investigation of the role of miR-29 on transcriptional responses to Mycobacterium tuberculosis (MTB) infection in human dendritic cells using gain- and loss-of-function approaches and microarray expression profiling. We assessed the impact of miR-29 perturbation on mRNA expression levels before and after MTB infection in dendritic cells using cells collected from 4 unrelated individuals. Cells were transfected using either a miR-29a mimic or miR-29 family inhibitor before infection with H37Rv for 24 hours. Gene expression was profiled by array and 4 technical replicates were performed to confirm reproducibility.

2014-01-17 | E-GEOD-53143 | biostudies-arrayexpress

miR-29 affect on DC gene expression

Project description:Transcriptional profiling of human monocyte-derived dendritic cells (MDDCs), comparing cells transfected with miR-29a mimic, or miR-29b mimic, or negative control.

2013-06-01 | GSE44784 | GEO

miR-29 affect on DC gene expression

Project description:Transcriptional profiling of human monocyte-derived dendritic cells (MDDCs), comparing cells transfected with miR-29a mimic, or miR-29b mimic, or negative control. 3 condition experiment, control versus miR-29a, and control versus miR-29b. 3 biological replicates for each condition and control.

2013-06-01 | E-GEOD-44784 | biostudies-arrayexpress

Illumina Bead expression array data from Human B cells treated with miR-29 over expression

Project description:Human Tonsillar B cells were isolated and transfected with miR-29 mimic molecules or transfection controls. B cells were subsequently cultured in class switching media for 24 hours and subjected to transcriptome analysis using the Illumina HumanHT-12 v4 Expression BeadChip array platform. B cells derived from 3 donors are submitted.

2020-06-24 | GSE100735 | GEO

Modulation of miR-29 influences myocardial compliance likely through coordinated regulation of calcium handling and extracellular matrix

Project description:MicroRNAs (miRs) control the expression of diverse subsets of target mRNAs, and studies have found miR dysregulation in failing hearts. Expression of miR-29 is abundant in heart, increased with aging, and altered in cardiomyopathies. Prior studies demonstrate that miR-29 reduction via genetic knockout or pharmacologic blockade can blunt cardiac hypertrophy and fibrosis in mice. Surprisingly, this depended on specifically blunting miR-29 actions in cardiomyocytes versus fibroblasts. To begin developing more translationally-relevant vectors, we generated a novel transgene-encoded miR-29 inhibitor (TuD-29) that can be incorporated into a viral-mediated gene therapy for cardioprotection. Herein, we corroborate that miR-29 expression and activity is higher in cardiomyocytes versus fibroblasts and demonstrate that TuD-29 effectively blunts hypertrophic responses in cultured cardiomyocytes and mouse hearts. Furthermore, we found that adeno-associated viral (AAV)-mediated miR-29 overexpression in mouse hearts induces early diastolic dysfunction, whereas AAV:TuD-29 treatment improves cardiac output by increasing end-diastolic and stroke volumes. Integration of RNA-seq and miR-target interactomes reveals that miR-29 regulates genes involved in calcium handling, cell stress and hypertrophy, metabolism, ion transport, and extracellular matrix remodeling. These investigations support a likely versatile role for miR-29 in influencing myocardial compliance and relaxation, potentially providing a unique therapeutic avenue to improve diastolic function in heart failure patients.

2023-11-21 | GSE241423 | GEO

MAPK-induced miR-29 targets MAFG and suppresses melanoma progression

Project description:The tumor suppressive miR-29 family of microRNAs is encoded by two clusters, miR-29b1~a and miR-29b2~c, and is regulated by several oncogenic and tumor suppressive stimuli. Here we investigated whether oncogenic MAPK hyperactivation regulates miR-29 abundance and how this signaling axis impacts melanoma development. Using mouse embryonic fibroblasts and human melanocytes, we found that oncogenic MAPK signaling stimulates p53-independent and p53-dependent transcription of pri-miR-29b1~a and pri-miR-29b2~c, respectively. Expression analyses revealed that while pri-miR-29a~b1 remains elevated, pri-miR-29b2~c levels decrease during melanoma progression. Using a rapid mouse modeling platform, we showed that inactivation of miR-29 in vivo accelerates the development of frank melanomas and decreases overall survival. We identified MAFG as a relevant miR-29 target that has oncogenic potential in melanocytes and is required for growth of melanoma cells. Our findings suggest that MAPK-driven miR-29 induction constitutes a tumor suppressive barrier by targeting MAFG, which is overcome by attenuation of miR-29b2~c expression.

2023-04-10 | GSE148552 | GEO

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